Modeling the MSX Parasite in Eastern Oyster (Crassostrea virginica) Populations. III. Regional Application and the Problem of Transmission

A model of transmission for Haplosporidium nelsoni, the disease agent for MSX disease, is developed and applied to sites in Delaware Bay and Chesapeake Bay. The environmental factors that force the oyster population- H. nelsoni model are salinity, temperature, food, and total suspended solids. The simulated development of MSX disease was verified using 3 time series of disease prevalence and intensity: 1960 to 1970 and 1980 to 1990 for Delaware Bay, and 1980 to 1994 for Chesapeake Bay, and for a series of sites covering the salinity gradient in each bay. Additional simulations consider the implications of assumptions made in development of the model for constraining the mode of transmission of H. nelsoni disease in oyster populations. Transmission of H. nelsoni includes non-local factors that exert a paramount influence on the transmission process. Key environmental forcing factors of season, salinity, and winter temperature exert a direct control on the transmission process, either by controlling the availability of infective particles in the water column or by controlling the population dynamics of an alternate host. Salinity\u27s role is a dual one. Salinity acts on the local host population by varying the infectivity of infective particles as they impinge the oyster gill during the filtration process. In addition, salinity exerts a regional influence on the transmission process by controlling, in part and on a bay-wide scale, the concentration of infective particles in the water column (or perhaps the abundance of an alternate host). In addition to the effect of salinity, infective particle concentration also decreases for 1 to 2 years after a cold winter and returns to high levels faster after a warm winter. It is the presence in the H. nelsoni transmission model of these bay-wide influences of environmental change that make this model different: from most other transmission models. Simulations suggest that epizootic cycles are principally the product of enhanced transmission rather than enhanced intensification. These influences of transmission on the course of infection, in many cases, have multiyear implications for prevalence and infection intensity, and the root of much of this multiyear behavior is in the processes that control the concentration of infective particles in the water column